Acute intraarticular trauma to weight-bearing joints--fracture, dislocation, sprain or internal derangement--is a common injury in Americans today, both young and old. The management of these injuries, whether by open surgery or conservative measures, is with the goal of restoration and preservation of pain-free, stable function. The development of traumatic arthritis, a result that is not always predictable, is a major cause in the development of a painful, unsatisfactory, and disabling joint. Experimentally, many intra- articular insults will produce degenerative disease as an end result; a "final common pathway" of joint destruction in arthritis of many etiologies has been postulated. Lysosomal hydrolases are implicated in cartilage degradation in arthritis, and elevated levels of these enzymes are demonstrable in articular tissues in established degenerative and inflammatory joint disease, both in patients and in experimental animals. The nature of the early synovial response to trauma has not been reported. We propose to study the synovial resoponse, in vitro and in vivo to acute intra-articular trauma in experimental animals over a period of 20 weeks. Intra-articular trauma, both with and without fracture, will be produced and these animals compared with animals subjected to standard procedures for creating degenerative or inflammatory arthritis. We propose to measure lysosomal enzyme levels in the synovium at specific intervals from injury, and to compare these levels among the various groups of animals, and to study the in vitro degradative potential of the synovium under these same conditions and correlate this potential with measured enzyme levels in the synovium and with histological and histochemical appearance of synovium and cartilge measured simultaneously.